shown that a person’s genes influence their exposure to 1) alcohol, and 2) their exposure to peers who use alcohol. In their study of 862 twin pairs, Fowler et al. (2007) found significant correlations (>0.60) between genetic influences on friends alcohol use and problem use and a person’s own use and problem use. Studies such as these indicate that individuals from high-risk backgrounds (i.e., alcohol abusing parents or relatives) may be more likely to place themselves in high-risk environments for AD (as seen above, interacting with substance abusing peers). If we are to obtain robust estimates of the contribution of genetic factors to the liability of alcohol dependence, the synergy between environmental factors and genetic factors must be acknowledged in molecular genetics approaches. In a previous report, Heath and Nelson (2002) highlighted the need for well-designed prospective studies and family-based association studies to identify important environmental risk factors and account for intergenerational processes that can confound the genetic risk for AD with other psychiatric disorders (Heath and Nelson, 2002). While there have been several advances in the environmental literature, our understanding of how genes and environments interact is still limited (Duncan and Keller, 2011). More importantly, environmental measures are not
